Evidence map›Paper›PMID 23969238›Full record

ReviewNeurobiology of disease2013

Role of calpains in the injury-induced dysfunction and degeneration of the mammalian axon.

Marek Ma

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Neuronal Calcium Signaling and Cytoskeletal Dynamics in Neurodegeneration.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. CaNeural regeneration research · 2023
    Article
  18. Review
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Marek MaDepartment of Emergency Medicine, University of Pennsylvania, Philadelphia, PA, USA; Center for Resuscitation Science, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: marek_ma@yahoo.com.
University of Pennsylvania · US

Funding

Calpain Activity in Traumatic Axonal Injury (Career Development Award)K08NS055880 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI MA, MAREK · 2006 to 2010
$866k
NINDS NIH HHS K08 NS055880NINDS NIH HHS K08NS055880
6 · The paper itself

Abstract

Axonal injury and degeneration, whether primary or secondary, contribute to the morbidity and mortality seen in many acquired and inherited central nervous system (CNS) and peripheral nervous system (PNS) disorders, such as traumatic brain injury, spinal cord injury, cerebral ischemia, neurodegenerative diseases, and peripheral neuropathies. The calpain family of proteases has been mechanistically linked to the dysfunction and degeneration of axons. While the direct mechanisms by which transection, mechanical strain, ischemia, or complement activation trigger intra-axonal calpain activity are likely different, the downstream effects of unregulated calpain activity may be similar in seemingly disparate diseases. In this review, a brief examination of axonal structure is followed by a focused overview of the calpain family. Finally, the mechanisms by which calpains may disrupt the axonal cytoskeleton, transport, and specialized domains (axon initial segment, nodes, and terminals) are discussed.

Indexed as

AxonsBrain InjuriesCalpainHumansSpinal Cord InjuriesCalpainAADacute axonal degenerationAISAMPAankGankyrinGAxonaxon initial segmentCalciumCalpainCAMCAPCasprCavcell adhesion moleculecentral nervous systemCMAPCNScommon small subunit 1common small subunit 2compound action potentialcompound muscle action potentialcontactin-associated proteinCSS1CSS2deoxyribonuclease Ideoxyribonucleic acidDICdifferential interference contrastDNADNase Idorsal root gangliaDRGdSarmEDLEGTAethylene glycol-bis(2-aminoethylether)-N,N,N′,N′-tetraacetic acidextensor digitorum longusGDCGFPgranular disintegration of the axonal cytoskeletongreen fluorescent proteinhorseradish peroxidaseHRPIAintra-arterialintraperitonealintravenousIPIschemiaIVKvMAPMCAOmicrotubule-associated proteinmiddle cerebral artery occlusionNa(+)–Ca(2+) exchangerNavNCXNeurofilamentneurofilament heavyneurofilament lightneurofilament mediumneuromuscular junctionneuronal cell adhesion moleculeNFHNFLNFMnicotinamide mononucleotide adenyl transferase 1Nmat-1NMJNodeNrCAMOGDoxygen glucose deprivationperipheral nervous systemPNSProteaseSCGSCIspinal cord injurysterile α/Armadillo/Toll–Interleukin receptor homology domain proteinsympathetic superior gangliaSynapseTAITBItetrodotoxinTraumatraumatic axonal injurytraumatic brain injuryTTXUbe4bubiquitination factor E4Bubiquitin–proteasome systemUPSvoltage-gated Ca(2+) channelvoltage-gated K(+) channelvoltage-gated Na(+) channelWallerian degenerationyellow fluorescent proteinYFPzinc and ring finger 1ZNRF1α-amino-3-hydroxy-5-methylisoxazole-4-propionateβ-amyloid precursor proteinβ-APP

Identifiers

PMID23969238
PMCPMC3882011
OpenAlexW1978713741

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.